| Project/Area Number |
17591481
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Thoracic surgery
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| Research Institution | Nagoya City University |
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Principal Investigator |
YANO Motoki Nagoya City University, Graduate School of Medical Sciences, Department of Oncology, Immunology and Surgery, Assistant professor, 大学院医学研究科, 講師 (40315883)
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| Co-Investigator(Kenkyū-buntansha) |
HANEDA Hiroshi Nagoya City University, Graduate School of Medical Sciences, Department of Oncology, Immunology and Surgery, Rinshoukenkyuui, 大学院医学研究科, 臨床研究医 (50381893)
ENDO Katsuhiko GNagoya City University, raduate School of Medical Sciences, Department of Oncology, Immunology and Surgery, Rinshoukenkyuui, 大学院医学研究科, 臨床研究医 (10381873)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2005: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | endostatin / antiangiogenesis / VEGF / VEGF受容体 / インテグリン |
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| Research Abstract |
We have established the endostatin transfection systems which showed the impact of antiangiogenesis and suppression of tumor growth. However the effect was not maintained for a long time. Finally the endostatin-tranfected animals died without tumor dormancy. There, also, have been no reports of effective clinical trials. We hypothesized the reasons he short effect of endostatin depended on up-regulation of some kinds of angiogenic factors. In the present study we have transfected mice lungs with endostatin gene and analyzed the VEGF gene expression. We used quantitative RT-PCR method to quantify the VEGF mRNA using GAPDH mRNA as an internal control. The both expression of Endostatin and VEGF mRNAs in the lung were apparent and the expression of VEGF mRNA in trasfection group (n=6) was higher than in cntol group (n=6) (p=0.0755 in Schffe's method in ANOVA, p=0.055 in Mann-Whitney U test). This mechanism was not unclear but the data was very important. This data may suggest that suppression of VEGF induced prolongation of effect of endostatin. Next we can try endostatin gene transfection with suppression of VEGF to prove the present data and achieve the tumor dormancy.
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